For the treatment of various diseases, it is often helpful to enhance the patient's natural blood circulation. It is particularly desirable to promote blood circulation in the treatment of ischemic diseases occurring in the extremities of limbs of the body. By artificially promoting blood circulation, the development of ischemic lesions on a patient's extremities may be curtailed and ischemic lesions that have already developed may be healed. Artificial promotion of blood circulation may also be used in the treatment of coronary heart disease, where it can be utilized to reduce myocardial ischemia and support left ventricle function, thereby increasing coronary artery perfusion and myocardial oxygen supply while reducing cardiac oxygen demand and work.
A non-invasive means of enhancing a patient's natural blood flow involves the use of devices which apply and remove pressure from at least a portion of the patient's extremity. For example, a patient's legs may be enclosed in air bags which may be inflated to apply pressure on the leg and deflated to remove pressure from the leg. Synchronous application of pressure on an extremity can enhance the flow of blood into the extremity, as well as enhancing the pumping of blood through the heart.
Intermittent compression of an extremity can improve the circulation in several ways. First, it facilitates return of interstitial fluid, i.e., lymph fluid or edema, from the extremities. Second, it facilitates venous return. If the venous valves are intact, venous back pressure on the capillary bed in the extremity is reduced to zero, thereby improving the arterial-venous gradient. Both of these actions may increase volume return to the heart, and neither is dependent upon timing the leg compression with the end-diastolic portion of the heartbeat.
End-diastolic intermittent pressure to an extremity provides several additional advantages, however. The first is the promotion of arterial flow in an ischemic extremity, such as a leg. The blood pulse wave is allowed to enter the leg, and compression provides a driving force to disseminate the blood through the tissues. Moreover, timing of compression with the end-diastolic portion of the heart cycle tends to augment the wave form that is reflected back from the compressed extremity. In a resting patient, the normal pulse wave that enters a leg, for example, wells up and is reflected backward toward the heart. Properly timed end-diastolic pumping applies pressure in addition to the normal pulse waves in the leg, which both disseminates blood in the leg and augments the reflected wave form. This augmentation of the reflected wave form can increase splanchnic, renal and coronary flow.
Properly timed end-diastolic pressure also has the potential of promoting aortic pulse wave harmonics. Decompressing the extremity in the presystolic phase of the heart cycle functions to drop the pressure in the inflatable enclosure, thereby creating a negative pressure gradient that effectively augments the reflected wave form from the aortic valve in presystole and decreases cardiac afterload. The diastolic timing of the compressions and their release in presystole thus augments normal pressure waves and allows the compression device to effectively operate at comfortable pressures, such as 55-70 mm Hg. Thus, end-diastolic intermittent pressure on an extremity has several positive effects on cardiac function. First, in preload phase, the blood returning to the heart from the peripheral circulation has a greater momentum, thereby enabling more efficient loading of the heart without as much work. Second, the decrease in afterload allows more complete emptying of the heart, thereby allowing the ejection fraction and cardiac output to increase, while decreasing heart work.
Intermittent external pressure on the extremity, when timed to the end-diastolic portion of the heart cycle has significant positive clinical effects. For example, patients may be relieved of heart failure. Their pulmonary edema may be relieved and their serum lactate/pyruvate ratio reduced. Patients with septic shock and lactic acidosis may also experience reduced blood lactate levels. Those patients with a murmur due to insufficiency of the mitral valve are found to have a decrease in the intensity of their murmur as more blood enters the aorta and legs, rather than being returned to the left atrium. Urinary output commonly increases in patients with prerenal azotemia. An increase in cardiac output per heartbeat is associated with a reflex slowing of the pulse rate in both sick and normal patients.
The observed effect of rescuing patients from acute myocardial infarction has been hypothesized to result from several factors. First, as described earlier, the work of the heart and its oxygen requirements are decreased when properly-timed intermittent compression of an extremity is applied. The observed increased ejection fraction of the heart probably signifies that stunned heart muscle is again contracting, thereby resuming the work of pumping blood. Additionally, intermittent compression of an extremity stimulates the formation of fibrinolysins in the blood, which may aid in dissolving coronary clots. Thus, the augmentation of preload and decrease in afterload can increase muscle contractions, mechanically moving and possibly squeezing the coronary arteries. This action, together with the stimulation of fibrinolysins, can help restore patency to coronary arteries blocked with thrombus.
To this end, U.S. Pat. Nos. 3,961,625, 4,269,175, 4,343,302 and 4,590,925 to the present inventor disclose methods and apparatus to provide end-diastolic intermittent pressure to one or more extremities. The above-referenced patents emphasize a unique timing that relates compressions of the extremity to the occurrence of the QRS complex in the EKG tracing, which represents electrical systole for the ventricles.
With respect to timing compression of the extremity to promote blood flow through the extremity, the time delay from the QRS complex to the entry of the blood pulse into the extremity must be taken into account. The application of pressure is typically set at a pre-determined variable interval after the QRS complex, and the release of pressure may be set at a pre-determined variable interval after application of the pressure, or it may be triggered by the next QRS complex.
The timing of application of pressure depends on the pulse rate of the patient and on the size of the extremity. Compression is preferably applied as late as possible in the diastolic portion of the heart cycle. However, because the pressure in the air bag must overcome the inertia of blood in the extremity, the time of inflation of the air bag must be sufficiently long to overcome this inertia. For circulation-promoting systems such as that described in U.S. Pat. No. 4,343,302, a compression time of no less than 0.34 seconds is necessary.
Thus, an intermittent external compression system, in order to provide effective promotion of circulation through an extremity, is regulated by a timing cycle comprising a time delay (time necessary from the QRS complex for the subsequent pulse wave to reach the extremity) and a compression period (time which the extremity is compressed to facilitate movement of the blood through the extremity). The compression period should be calculated and set on the basis of the size of the extremity, and the time delay should compensate for movement of the pulse from the heart to the extremity. Current systems accomplish this either by pre-setting the time delay and the compression period, so that the sum of the two is approximately equal to the time between QRS complexes, or by manually adjusting the time delay to take into account changes in heart rate. Neither of these current methods is adequate to assure effective pumping of blood through the extremities of patients having either a very rapid and/or an irregular heart rate, nor can they compensate for the normal slowing of the heart rate that accompanies intermittent pressure therapy. Currently, no method is available for adjusting the timing cycle to better coincide with QRS complexes of patients with variable heart rates. Clearly, in order for external intermittent pressure therapy to be fully effective in such cases, such a method is needed.
With respect to promoting the flow of blood through the heart, the timing of pressure and release on the extremity again is important. The first fraction of mechanical systole is an isometric contraction in which the muscle tightens around the contained blood, raising the pressure within the ventricle from a low level to the level of diastolic blood pressure. When the intraventricular pressure reaches diastolic blood pressure, the aortic valve opens and blood begins to leave the ventricle, as the ventricular chamber actually decreases in size. Electrical systole, hence, precedes the first movement of blood from the ventricles by approximately 0.05 seconds. Peak ventricular outflow occurs approximately 0.1 seconds later, or 0.15 seconds after the QRS complex occurs. Blood ejection from the ventricles ends with the closure of the aortic valve, which follows the QRS complex by about 0.24 seconds. Assuming that pulse waves from the extremity to the heart travel at approximately 20-40 feet per second (the rate at which they would travel in water, a noncompressible medium), the drop in pressure caused by release of compression on the extremity is perceived by the heart within approximately 0.1-0.15 seconds. In view of the fact that blood ejection from the ventricles takes approximately 0.24 seconds after the QRS complex, if the extremity is decompressed at the next QRS complex, and 0.1-0.15 seconds pass before the drop in pressure is perceived by the heart, the drop in aortic blood pressure due to the release of the extremity is perceived by the heart for perhaps only the last 2/3 of the systole. To facilitate complete unloading of the heart, however, it would be preferable if pressure to the extremity were released before the next occurring QRS complex, so that the drop in pressure perceived by the heart occurs for the entire duration of systole. This could be accomplished by triggering the decompression of the air bag either by the "P" wave (atrial systole), or by manually anticipating occurrence of the next QRS complex and triggering deflation of the air bag approximately 0.02-0.1 seconds earlier. The use of the "P" wave is limited to those patients having "p" waves. Patients with atrial fibrillation have no "P" waves.
Thus, promotion of blood circulation through the heart involves precise timing of decompression of the extremity to occur shortly (e.g., 0.02-0.1 seconds) before the next occurring QRS complex. Manual adjustment of the time delay, which is the method currently available to regulate compression and decompression with the QRS complex, is clearly a cumbersome and inadequate means to precisely control decompression of the extremity to enable complete unloading of the heart. Patients with rapid or irregular heart rates are particularly disadvantaged because it is extremely difficult to continuously adjust compression and decompression of the extremity to coincide with a particular instant in the QRS cycle. In promoting pumping of blood through the heart and through an extremity, then, a method of adjusting compression and decompression of the air bag would indeed be a marked improvement over the methods currently available.